The hapten-binding myelomas of BALB/c mice provide monoclonal populations of antigen-binding B cells that are responsive to immunoregulatory effectors induced in tumor-bearing hosts. Specific, immunological regulation of myeloma cell proliferation, differentiation, and immunoglobulin expression demonstrates many of the features that occur in T cell-mediated regulation of nonneoplastic antigen-binding B cells. Immunoregulation of MOPC-315 cell proliferation and immunoglobulin expression can be induced by: (1) immune response directed to the idiotypic antigens of M315 and (2) carrier specific presentation of TNP to the cell surface membrane TNP receptor of MOPC-315 celIs in carrier-primed syngeneic hosts. Immunization of BALB/c with M315 induces two distinct suppressor T-cell populations. One population mediates a cytostatic effect on MOPC-315 proliferation, and the other population inhibits M315 synthesis and secretion. In the past year, we have shown that inhibition of synthesis results from a specific and reversible suppression of light chain mRNA expression in MOPC-315 cells. We have shown that inhibition of synthesis results from a specific and reversible suppression of light chain mRNA expression in MOPC-315 cells. In the past year we have constructed a number of double-producing myeloma clones by fusing two different hapten-binding myeloma clones and selecting double-producers. This has generated a library of clones in which the partner immunoglobulins express the same or different heavy and/or light chains. In addition, kappa light chain genes have been successfully transfected into MOPC-315 cells to generate clones in which a constitutive lambda[unreadable]2[unreadable] light chain and the vectored kappa light chain are coexpressed. These cells will be examined to determine if light chain depression is light chain-class specific. The major objective of these studies is to develop an understanding of the immunological mechanisms that regulate the growth and differentiation of normal and neoplastic B cells. (IP)